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Review
. 2024 Aug 14;32(8):1264-1279.
doi: 10.1016/j.chom.2024.07.020.

Commensal microbe regulation of skin cells in disease

Yuyang Gan  1 , Jiarui Zhang  1 , Fangfang Qi  1 , Zhiqi Hu  1 , Evan Sweren  2 , Sashank K Reddy  3 , Lu Chen  1 , Xinyi Feng  1 , Elizabeth A Grice  4 , Luis A Garza  5 , Gaofeng Wang  6
Affiliations
Review

Commensal microbe regulation of skin cells in disease

Yuyang Gan et al. Cell Host Microbe. .

Abstract

Human skin is the host to various commensal microbes that constitute a substantial microbial community. The reciprocal communication between these microbial inhabitants and host cells upholds both the morphological and functional attributes of the skin layers, contributing indispensably to microenvironmental and tissue homeostasis. Thus, disruption of the skin barrier or imbalances in the microbial communities can exert profound effects on the behavior of host cells. This influence, mediated by the microbes themselves or their metabolites, manifests in diverse outcomes. In this review, we examine existing knowledge to provide insight into the nuanced behavior exhibited by the microbiota on skin cells in health and disease states. These interactions provide insight into potential cellular targets for future microbiota-based therapies to prevent and treat skin disease.

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Conflict of interest statement

Declaration of interests L.A.G. has received grant support paid to his institution, Johns Hopkins University, from Sun Pharma Advanced Research Company (SPARC). This grant is to investigate intellectual property of which Johns Hopkins University is the owner. L.A.G. is one of several inventors and is under a licensing agreement with SPARC; this intellectual property has resulted in royalty payments to inventors. This grant and the royalty payments are not related to the research presented in this manuscript.

Figures

Figure 1.
Figure 1.. Interaction between bacteria and cells during wound healing.
(A) Chronic wound. Various bacteria delay wound healing via increasing wound inflammation and inhibiting keratinocytes and fibroblasts. S. aureus: Staphylococcus aureus; A. baumannii: Acinetobacter baumannii; IL: Interleukin; TNF-α: Tumor necrosis factor alpha; SpA: Staphylococcus protein A; MMP-1: Matrix metalloproteinase-1; FB: Fibroblast; NET: Neutrophil extracellular trap; ECM: Extracellular matrix. (B) Acute wound. Positive regulation of cellular behavior by skin microbes that promote wound healing. S. epidermidis: Staphylococcus epidermidis; L. plantarum: Lactobacillus plantarum; HIF-1α: Hypoxia-Inducible Factor 1-alpha; LTA: Lipoteichoic acid; TLR: Toll-like receptor; AHR: Aryl hydrocarbon receptor; B2AR: β2-adrenergic receptor; AAA: Aromatic amino acid; TA: Trace amine; CXCL: C-X-C Motif Chemokine Ligand; pDC: Plasmacytoid dendritic cell; CD8+ Tc17: IL-17A+ CD8+ T cells; 1-IFN: Type 1 Interferon; MHC-I: Major Histocompatibility Complex class I; EV: Extracellular vesicle.
Figure 2.
Figure 2.. Interaction between bacteria and cells in inflammatory skin diseases.
(A) Psoriasis. Multiple microbes exacerbate inflammation by regulating keratinocytes and immune cells and participate in the maintenance of skin moisture in psoriasis. S. aureus: Staphylococcus aureus; C. acnes: Cutibacterium acnes; IL: Interleukin. (B) Atopic dermatitis. Skin microbes exacerbate inflammation and itching (left), disrupt the skin barrier (middle), and alleviate symptoms (right) of AD. S. epidermidis: Staphylococcus epidermidis; TLR: Toll-like receptor; NLRP1:NOD-like receptor family pyrin domain containing 1; IgE: Immunoglobulin E; EGFR: Epidermal growth factor receptor; ILC2: Innate lymphoid cell 2; PG: Phosphatidylglycerol antigen; Treg: Regulatory T cell; hBD: human β-Defensin; EV: Extracellular vesicle.
Figure 3.
Figure 3.. Interaction between bacteria and cells in diseases related to follicle-sebaceous gland niche.
(A) Alopecia. The imbalance of scalp microbes and the pathogenic mechanism in Androgenic alopecia (left) and Alopecia areata (right). AGA: Androgenic alopecia; AA: Alopecia areata; C. acnes: Cutibacterium acnes; IL-7R: Interleukin-7 Receptor; CCR6: C-C Chemokine Receptor Type 6; S1P1R: Sphingosine-1-Phosphate Receptor; IFN-γ: Interferon-γ. (B) Acne. Pathogenic C. acnes exacerbates skin inflammation by regulating keratinocytes, sebaceous gland cells, and various immune cells (left). S. epidermidis alleviates acne by releasing antimicrobial peptides and regulating keratinocytes (right). S. epidermidis: Staphylococcus epidermidis; CRH/CRH-R: Corticotropin releasing hormone/corticotropin releasing hormone receiver; IGF/IGF-R: Insulin-like growth factor-1/insulin like growth factor-1 receiver; IL:Interleukin; hBD-2: human β-Defensin-2; MMP: Matrix metalloproteinase; PAR-2: Protease-activated receptor-2; TLR: Toll-like receptor; ROS: Reactive oxygen species; CAMP: Cathelicidin; IFN-γ: Interferon-γ; AMP: Antimicrobial peptide; SA: Succinic acid; SMase: Sphingomyelinase; LTA: Lipoteichoic acid; miR-143: microRNA-143.
Figure 4.
Figure 4.. Prospects of future microbial therapy in different skin diseases.
Potential targeted cell behavior for future microbial therapy in different skin diseases. Wound (green): FB: Fibroblast; ILC: Innate lymphoid cell; TLR: Toll-like receptor; C5aR:C5a Receptor; IL: Interleukin; 3-IALD: Indole-3-aldehyde; TGF-β: Transforming growth factor β; SCFA: Short-chain fatty acid; GPR43: G protein-coupled receptor 43; NLRP3: NOD-like receptor family pyrin domain-containing protein 3; α-SMA: α-smooth muscle actin; AHR: Aryl hydrocarbon receptor; ER: Endoplasmic reticulum. Psoriasis (yellow): S. epidermidis: Staphylococcus epidermidis; C. acnes: Cutibacterium acnes; SMase: Sphingomyelinase; KC: Keratinocyte. Atopic dermatitis (brown): MRGPRX2: Mas-related G protein-coupled receptor X2; hBD: humanβ-Defensin; AHR: Aryl hydrocarbon receptor; TRPV1: Transient Receptor Potential Vanilloid 1; CCL11: Chemokine C-C motif ligand 11. Alopecia (purple): CCL20: Chemokine C-C motif ligand 20; CCR6: Chemokine C-C motif receptor 6; Treg: Regulatory T cell; HFSC: Hair Follicle Stem Cell; DHT: Dihydrotestosterone. Acne (blue).
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